METABOLIC SUPPRESSORS OF TRIMETHOPRIM AND ULTRAVIOLET-LIGHT SENSITIVITIES OF SACCHAROMYCES-CEREVISIAE RAD6 MUTANTS
METABOLIC SUPPRESSORS OF TRIMETHOPRIM AND ULTRAVIOLET-LIGHT SENSITIVITIES OF SACCHAROMYCES-CEREVISIAE RAD6 MUTANTS
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DOI：
10.1128/jb.139.3.866-876.1979
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发表时间：
1979-01-01
影响因子：
3.2
通讯作者：
CHRISTENSEN, RB
中科院分区：
文献类型：
--
作者：
LAWRENCE, CW;CHRISTENSEN, RB
在2个新鉴定的基因座，命名为SRS 1和SRS 2，代谢抑制rad 6和rad 18菌株的甲氧苄啶敏感性的显性突变，分离自酵母S的rad 6 -1 rad 18 -2菌株中自发产生的甲氧苄啶抗性突变体。啤酒。SRS 2突变还有效地抑制亲本菌株的UV光敏感性。它们不抑制其对电离辐射的敏感性或其在诱变和孢子形成方面的缺陷。这些观察结果支持了这样的假设，即RAD 6依赖性活动可以分为两个功能不同的组：一组负责野生型菌株的大量辐射抗性以及它们对甲氧苄啶的抗性的无错误修复活性，以及一组负责诱导诱变并且在孢子形成中也很重要的易错活性，但其最多仅占非常少量的野生型恢复。
Dominant mutations at 2 newly identified loci, designated SRS1 and SRS2, that metabolically suppress the trimethoprim sensitivity of rad6 and rad18 strains, were isolated from trimethoprim-resistant mutants arising spontaneously in rad6-1 rad18-2 strains of the yeast S. cerevisiae. The SRS2 mutations also efficiently suppress the UV light sensitivity of the parent strains. They do not suppress their sensitivity to ionizing radiation or their deficiency with respect to induced mutagenesis and sporulation. Such observations support the hypothesis that RAD6-dependent activities can be separated into two functionally distinct groups: a group of error-free repair activities that are responsible for a large amount of the radiation resistance of wild-type strains and also for their resistance to trimethoprim, and a group of error-prone activities that are responsible for induced mutagenesis and are also important in sporulation, but which account at best for only a very small amount of wild-type recovery.